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R Pumain

Publications and source records attributed to R Pumain.

At least 37 records · Page 2Linked to original sources
PubMed1990

Epileptiform activity induced by low chloride medium in the CA1 subfield of the hippocampal slice.

1. Extracellular and intracellular recordings and measurements of the extracellular concentration of free K+ ([K+]o) were performed in the CA1 subfield of the rat hippocampal slice during perfusion with artificial cerebrospinal fluid (ACSF) in which NaCl had been replaced with equimolar Na-isethionate or Na-methylsulfate (hereafter called low Cl- ACSF). 2. CAl pyramidal cells perfused with low Cl- ACSF generated intracellular epileptiform potentials in response to orthodromic, single-shock stimuli delivered in stratum (S.) radiatum. Low-intensity stimuli evoked a short-lasting epileptiform burst (SB) of action potentials that lasted 40-150 ms and was followed by a prolonged hyperpolarization. When the stimulus strength was increased, a long-lasting epileptiform burst (LB) appeared; it had a duration of 4-15 s and consisted of an early discharge of action potentials similar to the SB, followed by a prolonged, large-amplitude depolarizing plateau. The refractory period of the LB was longer than 20 s. SB and LB were also seen after stimulation of the alveus. 3. Variations of the membrane potential with injection of steady. DC current modified the shape of SB and LB. When microelectrodes filled with the lidocaine derivative QX-314 were used, the amplitudes of both SB and LB increased in a linear fashion during changes of the baseline membrane potential in the hyperpolarizing direction. The membrane input resistance, as measured by injecting brief square pulses of hyperpolarizing current, decreased by 65-80% during the long-lasting depolarizing plateau of LB. 4. A synchronous field potential and a transient increase in [K+]o accompanied the epileptiform responses. The extracellular counterpart of the SB was a burst of three to six population spikes and a small increase in [K+]o (less than or equal to 2 mM from a resting value of approximately 2.5 mM). The LB was associated with a large-amplitude, biphasic, negative field potential and a large increase in [K+]o (up to 12.4 mM above the resting value). Changes in [K+]o during the LB were largest at the border between S. oriens and S. pyramidale. This was also the site where the field potentials measured 2-5 s after the stimulus attained their maximal amplitude. Conversely, field potentials associated with the early component of the LB or with the SB displayed a maximal amplitude in the S. radiatum. 5. Spontaneous SBs and LBs were at times recorded in the CA1 and in the CA3 subfield.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Loss of N-methyl-D-aspartate sensitivity of cerebellar Purkinje cells after climbing fiber deafferentation. An in vivo study in the rat.

The sensitivity of cerebellar Purkinje cells to brief iontophoretic applications of excitatory amino acids has been studied in vivo in rats treated from 15 days to 4 months beforehand with 3-acetylpyridine in order to destroy the inferior olive. Responses of Purkinje cells (PCs) chronically deprived of climbing fibers were thus investigated using extracellular microelectrodes and compared to those of a group of control rats. No changes in the relative efficiencies of L-glutamate, L-aspartate, quisqualate and kainate have been observed. In contrast, the excitations induced by N-methyl-D-aspartate (NMDA) on most PCs in control animals, were no longer present after climbing fiber deprivation. These results show that both NMDA and non-NMDA receptors are present on PCs of adult rodents and that the NMDA responses are strongly depressed when PCs are deafferented of the climbing fibers.

Amino Acids↗
PubMed1989

Antidromic firing occurs spontaneously on thalamic relay neurons: triggering of somatic intrinsic burst discharges by ectopic action potentials.

Eighty-two identified thalamocortical relay neurons were recorded extracellularly in the ventral posterior thalamic nucleus in 29 urethane-anaesthetized rats. Electrical stimulations were applied to the contralateral vibrissae or to the ipsilateral neocortex for ortho- or antidromic activation. The critical period following a known somatic action potential and during which no antidromic response could reach the soma was systematically determined for each cell using a collision test. Thus, the possible ectopic axonal origin of a given impulse could be determined. Thalamic neurons displayed either tonic or phasic firing modes, the latter characterized by episodes of rhythmic high-frequency burst discharges. The present results suggest that such bursts were generated at the soma and probably involved an intrinsic mechanism, since: (1) a modulation of the somatic excitability with an excitatory or inhibitory amino acid affected the intra-burst structure; (2) an antidromic test action potential collided with the second or any of the later impulses of such bursts; (3) an orthodromic activation could evoke a burst structurally similar to a natural one; and (4) the duration of the first interval of such an evoked burst was always inferior to the sum of the critical period plus the antidromic conduction time, ruling out the possibility that it might have been entirely ectopically generated on thalamic terminals. The results further show that a spontaneous ectopic axonal impulse could trigger a somatic burst, since: (1) an electrically-evoked antidromic action potential could trigger a burst structurally similar to a spontaneous one; (2) on 42% of the tested thalamic cells, a known antidromic action potential delivered during the critical period following a spontaneous single impulse could not collide with it: in many cases such non-collisions were seen with the first action potential of a burst; and (3) with increasing ionophoretic doses, GABA could: (i) convert bursts to single action potentials, while the ortho- but not the antidromic responses were abolished, (ii) block these single impulses at similar doses than those which abolished known antidromic ones, and (iii) multiply by a factor of 3 the probability of testing an ectopic action potential. On 70% of the cells tested, such GABA-isolated impulses could be proved to have been ectopically generated. Finally, ectopic impulses have never been observed during periods of tonic firing, indicating that such a feature was not an experimental artifact.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1987

Seizure-like discharges induced by lowering [Mg2+]o in the human epileptogenic neocortex maintained in vitro.

Seizure-like discharges were observed in slices of human epileptogenic neocortex maintained in vitro when [Mg2+]o was lowered near to zero. This type of epileptiform activity: (1) could occur spontaneously or following extracellular focal stimuli; (2) resembled the electrographic pattern associated with tonic-clonic seizures; (3) was accompanied by increases in [K+]o (maximally 6.2 mM from a baseline of 3.25 mM) and decreases in [Ca2+]o (maximally 0.23 mM from a baseline of 1.8 mM). Application of the selective antagonist of N-methyl-D-aspartate (NMDA) receptors, DL-2-amino-5-phosphonovalerate, suppressed in a reversible manner both spontaneous and stimulus-induced seizure-like discharges, suggesting that NMDA-activated conductances are important for the genesis of prolonged epileptiform discharges generated by human epileptogenic neocortical slices.

Epilepsies, Partial↗
PubMed1987

Ionic changes induced by excitatory amino acids in the rat cerebral cortex.

The ionic mechanisms underlying the action of excitatory amino acids were investigated in the rat motor cortex. Ion-selective microelectrodes were attached to micropipettes such that their tips were very close and local changes in extracellular concentration of sodium, calcium, and potassium ions elicited through ionophoretic applications of glutamate (Glu) and of its agonists N-methyl-D-aspartate (NMDA), quisqualate (Quis), and kainate (Ka) were measured. These agents produced moderate increases in [K+]o (up to 13 mM) but, in contrast, substantial tetrodotoxin-insensitive decreases in [Na+]o (maximally of 60 mM). NMDA-induced sodium responses could be blocked by manganese, while the Quis- and Ka-induced responses were not. Quis and Ka produced increases in [Ca2+]o or biphasic responses while NMDA, even with small doses, induced each time drastic decreases in [Ca2+]o (maximally of 1.15 mM), which could be attenuated or blocked by manganese but not by organic calcium channel blockers. NMDA responses could be abolished by reduced doses of 2-amino-phosphonovalerate. The largest Glu- and NMDA-induced calcium responses were observed in the superficial cortical layers, but such maxima disappeared after selective degeneration of pyramidal tract neurons. All amino acids produced sizeable reductions in the extracellular space volume. The following can be concluded. (i) All the excitatory amino acids tested induce an increased permeability to sodium and potassium ions. (ii) In addition, the NMDA-operated channels have specifically a large permeability for calcium, although calcium ions contribute only by less than 10% to the NMDA-induced inward currents.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1986

Long-term alterations in amino acid-induced ionic conductances in chronic epilepsy.

Extracellular free sodium (Na+)o and calcium (Ca2+)o concentration changes were measured in the rat motor cortex, using ion-selective microelectrodes. During ionophoretic applications of excitatory amino acids, decreases in (Na2+)o and in (Ca2+)o were observed. Ca2+ signals were not or very little modified by applications of tetrodotoxin while Na+ signals were slightly depressed, up to 20%. Laminar profile analysis revealed that, while the magnitude of Na+ signals was rather constant throughout the cortex, Ca2+ signals were largest in upper cortical layers. Lesioning and pharmacological experiments indicated that the corresponding permeabilities were most probably located on apical dendrites of pyramidal tract neurons. The relative amplitude of Na+ and Ca2+ signals induced by the release of the glutamate agonists N-methyl-D-aspartate, quisqualate and kainate and the shape of the laminar profile of such responses indicated that different ionic permeabilities located on different neurons underlie such responses. Similar experiments performed on chronic epileptogenic motor foci in rats indicated that the amino acid-induced ionic responses were altered. The significance of such alterations for epileptogenesis is discussed.

Amino Acids↗
PubMed1986

Extracellular calcium and potassium concentration changes in chronic epileptic brain tissue.

Repetitive electrical stimulation and application of excitatory amino acids lead to decreases in extracellular Ca2+ concentration and to rises in extracellular K+ concentration [( Ca2+]o, [K+]o) with a typical laminar distribution in a given neo- or allocortical structure. These ionic changes result from transmembrane ion fluxes along their respective electrochemical gradients. Epileptogenic drugs that impair repolarizing K+ conductances or inhibitory synaptic transmission enhance such extracellular ionic changes, but they do not alter the laminar distribution of [K+]o and [Ca2+]o changes. Enhanced [Ca2+]o concentration changes are also observed in chronic epilepsies such as the chronic alumina cream and cobalt focus, the kindling epilepsy, and during photically induced seizures in the baboon Papio papio. In chronic epilepsies, the sites of maximal [Ca2+]o changes shift to other layers, suggesting changes in the distribution of ion channels over the surface of nerve cells that may be involved in epileptogenesis in chronic epilepsies. The K+ and Ca2+ concentration changes associated with seizure contribute to the generation and spread of epileptic activity. This is demonstrated by the fact that lowering of extracellular free calcium concentration can induce spreading epileptiform activity in the absence of chemical synaptic transmission, with [K+]o rises preceding epileptiform activity.

Aluminum Oxide↗
PubMed1985

Ectopic action potential generation: its occurrence in a chronic epileptogenic focus.

Intracortical axon terminals of thalamocortical relay neurons projecting into chronic cortical epileptogenic foci may generate high frequency bursts of action potentials during spontaneous cortical epileptiform paroxysms. Such bursts occur regularly before onset of the corresponding surface paroxysms in a large proportion of the tested neurons. Therefore, such axon terminals bursting may participate in the triggering of the synchronous, prolonged intracellular depolarization shifts which are observed in cortical neurons during epileptic events.

Action Potentials↗
PubMed1985

Chemical synaptic transmission is not necessary for epileptic seizures to persist in the baboon Papio papio.

The spread and persistence of epileptic seizures have generally been attributed to chemical synaptic interactions. Using ion-sensitive microelectrodes, we showed that in the allylglycine-treated photosensitive baboon, prolonged light-induced generalized seizures were accompanied by abnormally large decreases in the concentration of extracellular calcium ions, reaching values at which chemical synaptic transmission was certainly very reduced or blocked. This feature was observed in all cortical layers. Measurements of the concentration of extracellular potassium ions in the course of such light-induced seizures indicated that the observed low values of the concentration of calcium ions could not be ascribed to the occurrence of spreading depressions. These findings showed that nonsynaptic mechanisms play a prominent role in the persistence of epileptic seizures.

Animals↗
PubMed1985

Stimulus- and amino acid-induced calcium and potassium changes in rat neocortex.

Local changes in extracellular concentration of calcium ions, [Ca2+]o, and potassium ions, [K+]o, elicited through ionophoretic applications of the excitatory amino acids glutamate (Glu) and aspartate (Asp) or through cortical surface stimulations were measured in the rat motor cortex using paired ion-selective microelectrodes. Glu or Asp applications produced dose-dependent decreases in [Ca2+]o from a base line of 1.25 mM to as low as 0.08 mM and increases in [K+]o from 2.8 mM to as high as 13.3 mM. These ionic changes were accompanied by negative DC potential shifts of up to 15 mV. [K+]o changes were practically constant in all cortical layers, whereas [Ca2+]o changes were variable with depth, showing two localized marked maximums. One was observed in the superficial layers, 150-300 microns below cortical surface and the second at 1,100-1,300 microns, in a region corresponding roughly to layer V. Application of tetrodotoxin (TTX) onto the cortical surface abolished stimulus-evoked ionic changes, whereas amino acid-induced [Ca2+]o changes remained practically unaltered, and [K+]o changes were reduced by 20% on average. Selective degeneration of the pyramidal tract neurons was induced by performing chronic lesions of the pyramidal tract at the bulbar level. In these conditions, laminar profiles of amino acid-induced [Ca2+]o changes were considerably altered in the corresponding motor cortex. The maximum Ca2+ changes were then reduced by two-thirds, and the [Ca2+]o signals were practically constant throughout the cortex. Local cobalt (Co2+) or manganese (Mn2+) applications could abolish amino acid-evoked [Ca2+]o changes, whereas most of the [K+]o changes persisted. gamma-Aminobutyric acid applications could decrease [Ca2+]o signals to a large extent, whereas [K+]o changes were diminished by only 15-25% on average. These results show that the putative neurotransmitters Glu and Asp induce significant changes in [Ca2+]o and [K+]o in the rat cerebral cortex and indicate the possible origin of the ion fluxes in terms of neuronal elements and ionic channels: in particular, they indicate that the major part of the amino acid-induced [Ca2+]o maximum decreases can be ascribed to Ca2+ movements through channels located very likely on the pyramidal tract neurons in the motor cortex. They also indicate that significant reductions of the extracellular space volume occur during excitatory amino acid applications.

Amino Acids↗
PubMed1983

Fast extracellular calcium transients: involvement in epileptic processes.

Improved liquid ion-exchanger microelectrodes made possible the observation of large, rapid decreases in the concentration of extracellular calcium ions during single epileptic spikes. Moreover, in definite cortical layers the decreases regularly started shortly before the onset of each epileptic spike. In view of the prominent role played by extracellular calcium ions in neuronal processes, including transmitter release and membrane excitability, these alterations probably exert a profound influence on the cellular events underlying epileptiform activity.

Action Potentials↗
PubMed1981

Electrophysiological abnormalities in chronic epileptogenic foci: an intracellular study.

Intracellular recordings were performed from chronic cobalt epileptogenic foci in rats. Two main features were found: (a) in 29% of the neurons, depolarizations of long duration occurred coinciding with cortical surface paroxysms; and (b) in 13% of the neurons, partial spikes, whose amplitude varied little with membrane DC potential changes, occurred. It is suggested that these phenomena have a dendritic origin, and possible mechanisms underlying the generation of paroxysmal events are discussed.

Animals↗
PubMed1981

Effects of tetrodotoxin on changes in extracellular free calcium induced by repetitive electrical stimulation and iontophoretic application of excitatory amino acids in the sensorimotor cortex of cats.

Extracellular free calcium ([Ca2+]o) was measured with double barreled ion-sensitive reference electrodes in the sensorimotor cortex of cats before and after application of tetrodotoxin (TTX). Electrical stimulation of the cortical surface or of the thalamic ventrobasal complex resulted in reductions of [Ca2+]o (delta Ca) by up to 0.45 mM (baseline 1.2--1.3 mM). Iontophoretic applications of the excitatory amino acids glutamate, aspartate and DL-homocysteate evoked delta Ca by up to 1.2 mM. delta Ca were largest at a depth of 100-300 micron below cortical surface. After application of 10(-5) M TTX to the cortical surface, the delta Ca evoked by electrical stimulation disappeared and the accompanying slow negative potentials were reduced in amplitude. In contrast, delta Ca evoked by excitatory amino acids were only slightly affected. It is suggested that excitatory amino acids activate voltage-dependent postsynaptic Ca2+ conductances in neocortical neurones.

Amino Acids↗
PubMed1980

Extracellular calcium activity changes in cat sensorimotor cortex induced by iontophoretic application of aminoacids.

Extracellular Ca2+ activity (aCa) changes were measured with Ca2+-sensitive microelectrodes in the cat cerebral cortex during iontophoretic administration of excitatory and inhibitory aminoacids. Glutamate, aspartate and DL homcysteate usually decreased aCa from a baseline of 1.3 mM to as low as 0.1 mM. The amplitude of the changes was largest at depths between 100 and 300 micrometer beneath the cortical surface. The aCa decreases could be deminished or blocked by Co2+, Mn2+ or La3+ as well as by GABA. These data suggest that large Ca2+ conductances that may be voltage-sensitive are present in apical dendrites of neocortical neurones.

Amino Acids↗